Several skin diseases (e.g., psoriasis) are strongly associated with HLA-D alleles. The explanation for these associations remains uncertain and forms the basis for this proposal. I have shown that human keratinocytes isolated from normal skin express HLD-D/DR antigens on their surface. Further, I have shown that keratinocytes can reconstitute this antigen after trypsinization and can be separated into DR positive and DR negative populations using the fluorescence activated cell sorter. Moreover, suspensions of epidermal cells synthesize HLA-DR antigen in vitro and two dimensional gels of immuno-precipitates of 35S-methionine labeled extracts of these cells give electrophoretic patterns indistinguishable from those obtained with extracts from B-lymphocytes. I propose to determine whether the staining pattern with monoclonal antibody against HLA-DR in skin specimens obtained from involved skin of patients with psoriasis and lichen planus differs from the staining pattern found in uninvolved and normal skin. Further, I plan to compare the structure of DR antigens present on involved and uninvolved skin from patients with skin disease using two-dimensional gel electrophoresis. Using this method, I also intend to compare the HLA-DR antigens on epidermal cells with those on lymphocytes in normal individuals and patients with skin disease. The epidermis produces a thymopoietin-like substance and cultured epidermal cells cause the differentiation of peripheral blood null cells into T lymphocytes. Both psoriasis and lichen planus histologically demonstrate a dermal infiltrate of mononuclear leukocytes, which in the case of psoriasis remain uncharacterized and in lichen planus have been shown to be T cells. I propose to define the particular subtype of lymphocytes present in the dermal infiltrate of both diseases using monoclonal antibodies against HLA-DR and against human T cells.